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We hypothesized that a genetic variant resulting in antioxidant insufficiency or pancreatic dysfunction would be responsible for high GGT syndrome in TBs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Animals<\/jats:title>\n                    <jats:p>A total of 138 California racing TBs. Amylase: n\u00a0=\u00a031 affected (serum GGT activity \u226560\u2009IU\/L), n\u00a0=\u00a052 control (serum GGT activity &amp;lt;40\u2009IU\/L). Lipase: n\u00a0=\u00a019 affected, n\u00a0=\u00a035 control. Serum \u03b1-tocopherol concentrations: n\u00a0=\u00a032 affected, n\u00a0=\u00a046 control. Genome-wide association study (GWAS): 36 affected, 58 control. Whole genome sequencing: n\u00a0=\u00a05 affected, n\u00a0=\u00a05 control.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Biochemical and vitamin analytes were compared among cohorts. A GWAS was performed and a subset of TBs underwent whole genome sequencing to interrogate candidate genes and positional genetic regions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Serum lipase and amylase activity and \u03b1-tocopherol concentrations did not differ between groups. No genetic variants were identified in 2 candidate genes (UGT1A1 and GGT1) that associated with the phenotype. Four single nucleotide polymorphisms (SNPs) approached a suggestive association with the phenotype (P\u00a0=\u00a02.15\u2009\u00d7\u200910\u22125), defining a 100\u2009kb region on chromosome 5 surrounding cluster of differentiation 1a (CD1A1), a transmembrane gene related to the major histocompatibility complex.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Clinical Importance<\/jats:title>\n                    <jats:p>An underlying genetic etiology may exist for high GGT syndrome in racing TBs, similar to genetic disorders in humans.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jvim.16582","type":"journal-article","created":{"date-parts":[[2022,11,15]],"date-time":"2022-11-15T05:45:50Z","timestamp":1668491150000},"page":"2203-2212","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Investigation of high gamma-glutamyltransferase syndrome in California Thoroughbred racehorses"],"prefix":"10.1093","volume":"36","author":[{"given":"Sichong","family":"Peng","sequence":"first","affiliation":[{"name":"University of California Department of Population Health and Reproduction, , Davis, California,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9988-3381","authenticated-orcid":false,"given":"K. 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